Background: Acute infection hepatitis C virus (HCV) is usually asymptomatic, making early diagnosis difficult. Approximately 70% of acutely infected individuals fail to clear the virus and become chronically infected. Chronic HCV infection is the leading cause of the development of liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC) and is the primary cause for liver transplantation in the Western world. Recent evidence indicates that HCV-associated insulin resistance may result in hepatic fibrosis, steatosis, HCC, and resistance to anti-viral treatment.

Methods: We performed a cross sectional population based study, on a representative sample of mexican adults aged 30 to 65 years. Anthropometric measurements of obesity that included waist circumference (WC) and total body fat percentage were collected and the body mass index calculated. All subjects also underwent an oral glucose tolerance test. Diagnosis of glucose metabolism disorders was based on criteria of the American Diabetes Association and HCV associated insulin resistance and also performed liver ALT test.

Results: In our study in Mexican population, the prevalence of altered fasting glycemia (AGA), impaired glucose intolerance (IGT), and AGA + IGT was 24.6, 8.3, and 10.3%, respectively. Thus, HCV-associated insulin resistance is a therapeutic target at any stage of HCV infection. HCV modulates normal cellular gene expression and interferes with the insulin signaling pathway. Glucose is a key metabolite essential for the production of energy (mostly ATP) which is required by cells.

Conclusions: Prevalence of prediabetes in the Mexican adult population is high. WC is the measure of obesity more strongly associated with metabolic glucose disorders. HCV and prediabetes has a insulin resistance. There are several mechanisms underlying increased glucose production. These include the production of free glucose by increased glycogenolysis in the liver, increased gluconeogenesis, activation of transcription factor (FoxO1), and improper insulin-glucagon hormonal balance, which stimulates increased glucose production.